The cause of psoriasis and atopic skin diseases has not been revealed clearly; however, those diseases are evaluated as allergic skin diseases. Atopic dermatitis is regarded as being related to genetic factors and immune system deficiency. Other than that, it has been reported that dry skin, characteristics of easily feeling itchy as compared with normal people, or emotional and environmental factors occur in combination with one another.
Atopic dermatitis patient-related lesion is related to overproduction of IL-6, IL-8 and IL-10 by a Th2-cell mediated immune response, and increased concentration of serum immunoglobulin (IgE), and decreased production of interferon-gamma (IFN-γ). Psoriasis is an immune-mediated-autoimmune skin disease induced by chronic activation of inflammatory cell infiltration in skin and control disorder of epidermal keratinocytes. According to the existing reports, it has been reported to be related to a complex mechanism including interaction between inflammatory cytokine and immune cellular infiltration such as T cells, and recently, it has been reported that not only Th1 cells, but also Th17 cells and Th-17-mediated cytokines such as IL-17A and IL-22 induce psoriasis promotion.
Meanwhile, autophagy refers to a mechanism to degrade aged or damaged intracellular constituents and organelles when intracellular energy source is depleted or intracellular stress factors are excessively generated, thereby regenerating energy and removing damaged constituents, and allows maintenance of normal cells. Recently, it has been reported through various studies that as aging proceeds, or aging is accelerated, intracellular autophagy activation is rapidly reduced. In addition, when the autophagy inhibition is occurred, the aged mitochondria and misfolded protein or the like is excessively accumulated in cells that results in the increases of free radicals and oxidative stress in cells, eventually leading to apoptosis and aging promotion.
Therefore, unfolded or misfolded proteins, excessive lipid droplets, damaged mitochondrias and the like are rapidly removed by activation of an autophagic mechanism which degrades intracellular aged constituents and organelles and recycles the decomposed product therefrom, thereby providing the environment where cells may survive in a more healthy state.
It is known from preceding reports that the autophagy modulation can be applied for the treatment and prevention of type II diabetes, as well as neurodegenerative diseases such as Alzheimer's disease, Huntington's disease and Parkinson's disease.
In addition, the autophagy maintains intracellular homeostasis, and is also related to an immune cell response and an inflammatory pathway. A mechanism for removing intracellular microorganisms is provided by autophagic adapters. Thus, there is a need to develop an autophagy activation material to treat and prevent neurodegenerative diseases and type II diabetes, and alleviate skin inflammation, by promoting intracellular autophagy activation.